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BACKGROUND: Cooking-related biomass smoke is a major source of household air pollution (HAP) and an important health hazard. Prior studies identified associations between HAP exposure and childhood stunting; less is known for underweight and wasting. Few studies had personal HAP measurements. METHODS: 557 households in rural Guatemala were enrolled in the CRECER study, the follow-up study of the RESPIRE randomized intervention trial. They were assigned to three groups that received chimney stoves at different ages of the study children. Multiple personal carbon monoxide (CO) exposure measurements were used as proxies for HAP exposures. Children's heights and weights were measured from 24 to 60 months of age. Height-for-age z-score (HAZ), weight-for-age z-score (WAZ), and weight-for-height z-score (WHZ) were calculated based on the World Health Organization's Multicentre Growth Reference Study. HAZ, WAZ, and WHZ below -2 were classified as stunting, underweight, and wasting, respectively. Generalized linear models and mixed effects models were applied. RESULTS: 541 children had valid anthropometric data, among whom 488 (90.2 %) were stunted, 192 (35.5 %) were underweight, and 2 (0.3 %) were wasted. A 1 ppm higher average CO exposure was associated with a 0.21 lower HAZ (95 % CI: 0.17-0.25), a 0.13 lower WAZ (95 % CI: 0.10-0.17) and a 0.06 lower WHZ (95 % CI: 0.02-0.10).The associations for HAZ were stronger among boys (coefficient = -0.29, 95 % CI: -0.35 - -0.22) than among girls (coefficient = -0.15, 95 % CI: -0.20 - -0.10). A 1 ppm-year higher cumulative CO exposure was associated with a higher risk of moderate stunting among boys (OR = 1.27, 95 % CI: 1.05-1.59), but not among girls. DISCUSSION: In this rural Guatemalan population, higher HAP exposure was associated with lower HAZ and WAZ. The associations between HAP and HAZ/stunting were stronger among boys. Reducing HAP might benefit childhood somatic growth in rural populations of low-income countries.
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Transtornos do Crescimento , Fumaça , Feminino , Humanos , Lactente , Masculino , Biomassa , Seguimentos , Transtornos do Crescimento/epidemiologia , Guatemala/epidemiologia , Estudos Prospectivos , População Rural , Fumaça/efeitos adversos , Magreza/epidemiologia , Pré-EscolarRESUMO
Women and children in rural regions of low-income countries are exposed to high levels of household air pollution (HAP) as they traditionally tend to household chores such as cooking with biomass fuels. Early life exposure to air pollution is associated with aeroallergen sensitization and developing allergic diseases at older ages. This prospective cohort study assigned HAP-reducing chimney stoves to 557 households in rural Guatemala at different ages of the study children. The children's air pollution exposure was measured using personal CO diffusion tubes. Allergic outcomes at 4-5 years old were assessed using skin prick tests and International Study of Asthma and Allergies in Childhood (ISAAC)-based questionnaires. Children assigned to improved stoves before 6 months old had the lowest HAP exposure compared to the other groups. Longer exposure to the unimproved stoves was associated with higher risks of maternal-reported allergic asthma (OR = 2.42, 95% CI: 1.11-5.48) and rhinitis symptoms (OR = 2.01, 95% CI: 1.13-3.58). No significant association was found for sensitization to common allergens such as dust mites and cockroaches based on skin prick tests. Reducing HAP by improving biomass burning conditions might be beneficial in preventing allergic diseases among children in rural low-income populations.
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Poluição do Ar em Ambientes Fechados , Asma , Hipersensibilidade , Criança , Humanos , Feminino , Pré-Escolar , Lactente , Poluição do Ar em Ambientes Fechados/efeitos adversos , Poluição do Ar em Ambientes Fechados/análise , Biomassa , Estudos Prospectivos , Guatemala/epidemiologia , Culinária , Alérgenos , Asma/epidemiologia , Asma/etiologia , Fumaça/efeitos adversosRESUMO
Chronic exposure to indoor biomass smoke from the combustion of solid organic fuels is a major cause of disease burden worldwide. Almost 3 billion people use solid fuels such as wood, charcoal, and crop residues for indoor cooking and heating, accounting for approximately 50% of all households and 90% of rural households globally. Biomass smoke contains many hazardous pollutants, resulting in household air pollution (HAP) exposure that often exceeds international standards. Long-term biomass-smoke exposure is associated with Chronic Obstructive Pulmonary Disease (COPD) in adults, a leading cause of morbidity and mortality worldwide, chronic bronchitis, and other lung conditions. Biomass smoke-associated COPD differs from the best-known cigarette smoke-induced COPD in several aspects, such as a slower decline in lung function, greater airway involvement, and less emphysema, which suggests a different phenotype and pathophysiology. Despite the high burden of biomass-associated COPD, the molecular, genetic, and epigenetic mechanisms underlying its pathogenesis are poorly understood. This review describes the pathogenic mechanisms potentially involved in lung damage, the development of COPD associated with wood-derived smoke exposure, and the influence of genetic and epigenetic factors on the development of this disease.
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Poluição do Ar em Ambientes Fechados , MicroRNAs , Doença Pulmonar Obstrutiva Crônica , Humanos , MicroRNAs/genética , Biomassa , Poluição do Ar em Ambientes Fechados/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/genética , Inflamação/genética , Inflamação/complicações , Pulmão , Estresse Oxidativo/genética , Polimorfismo GenéticoRESUMO
In barely nine months, the pandemic known as COVID-19 has spread over 200 countries, affecting more than 22 million people and causing over than 786 000 deaths. Elderly people and patients with previous comorbidities such as hypertension and diabetes are at an increased risk to suffer a poor prognosis after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Although the same could be expected from patients with chronic obstructive pulmonary disease (COPD), current epidemiological data are conflicting. This could lead to a reduction of precautionary measures in these patients, in the context of a particularly complex global health crisis. Most COPD patients have a long history of smoking or exposure to other harmful particles or gases, capable of impairing pulmonary defences even years after the absence of exposure. Moreover, COPD is characterized by an ongoing immune dysfunction, which affects both pulmonary and systemic cellular and molecular inflammatory mediators. Consequently, increased susceptibility to viral respiratory infections have been reported in COPD, often worsened by bacterial co-infections and leading to serious clinical outcomes. The present paper is an up-to-date review that discusses the available research regarding the implications of coronavirus infection in COPD. Although validation in large studies is still needed, COPD likely increases SARS-CoV-2 susceptibility and increases COVID-19 severity. Hence, specific mechanisms to monitor and assess COPD patients should be addressed in the current pandemic.
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Infecções por Coronavirus/epidemiologia , Pneumonia Viral/epidemiologia , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Betacoronavirus , Biomassa , COVID-19 , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/fisiopatologia , Suscetibilidade a Doenças , Exposição Ambiental/estatística & dados numéricos , Predisposição Genética para Doença , Humanos , Pandemias , Material Particulado , Pneumonia Viral/imunologia , Pneumonia Viral/fisiopatologia , Doença Pulmonar Obstrutiva Crônica/genética , Doença Pulmonar Obstrutiva Crônica/imunologia , SARS-CoV-2 , Índice de Gravidade de Doença , Fumaça , Fumar/epidemiologia , Fumar/imunologiaRESUMO
INTRODUCTION: Exposure to biomass smoke, cigarettes, alcohol, and the impairment of immunoregulation are considered to be risk factors for tuberculosis. Tumour necrosis factor (TNF) -308G/A and -238G/A gene polymorphisms have been associated with tuberculosis. However, the results remain inconsistent. The aim of this study was to determine the association between TNF polymorphisms and tuberculosis in the presence of biomass smoke, cigarettes, and alcohol in a Mexican population. MATERIAL AND METHODS: TNF polymorphisms were determined in 118 tuberculosis patients and 223 controls. We performed a univariate, bivariate, stratified analysis. Odds ratios, confidence intervals, and p-values were calculated. RESULTS: Occupational biomass smoke exposure was associated with tuberculosis between the patients and controls (OR = 1.70, 95% CI: 1.08-2.70, p = 0.02). We also found an association of the -308A allele carriers between the patients and controls without exposure to occupational (p = 0.04, OR = 0.16, 95% CI: 0.01-0.92) and in-home (p = 0.02, OR = 0.14, 95% CI: 0.01-0.81) biomass smoke, as well as an association with alcohol (p = 0.01, OR = 0.24, 95% CI: 0.05-0.75). The haplotype analysis revealed an association of the -308A/-238G haplotype between patients and nonconsanguineous controls without exposure to occupational (p = 0.02, OR = 0.12, 95% CI: 0.01-0.99) and in-home (p = 0.01, OR = 0.1, 95% CI: 0.01-0.9) biomass smoke, cigarette use (p = 0.04, OR = 0.28, 95% CI: 0.08-0.98), and alcohol (p = 0.02, OR = 0.22, 95% CI: 0.05-0.88) intake. CONCLUSIONS: The TNF -308A allele and the -308A/-238G haplotype are associated with tuberculosis, as are exposure to biomass smoke, cigarettes, and alcohol. No association for the -238G/A polymorphism was found. Our results provide insight into a possible protective role of TNF polymorphisms in tuberculosis in our population.
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Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation and systemic inflammation. The main causes of COPD include interaction between genetic and environmental factors associated with tobacco smoking (COPD-TS) and/or exposure to biomass smoke (COPD-BS). Several microRNAs (miRNAs) control posttranscriptional regulation of COPD-TS associated gene expression. The miR-22-HDAC4-IL-17 axis was recently characterized. It is still unknown, however, whether this axis, participates in COPD-BS. To investigate, 50 patients diagnosed with severe-to-very severe COPD GOLD (Global Initiative for Chronic Obstructive Lung Disease) stages III/IV, were recruited, 25 women had COPD-BS (never smokers, exposed heavily to BS) and 25 had COPD-TS. Serum levels of miRNA-22-3p were measured by RT (Reverse Transcription)-qPCR, while the concentration of HDAC4 (Histone deacetylase 4) was detected by ELISA. Additionally, we looked for association between serum HDAC4 and DLCOsb (Single-breath diffusing capacity of the lung for carbon monoxide), as % of predicted by age, height, and gender, one of the main differences described between COPD-BS and COPD-TS. Women with COPD-BS were older and shorter and had a higher DLCOsb %P (percent predicted) compared to COPD-TS. Serum miR-22-3p was downregulated in COPD-BS relative to COPD-TS. In contrast, the concentration of HDAC4 was higher in COPD-BS compared to COPD-TS. Furthermore, a positive correlation between serum HDAC4 levels and DLCOsb %P was observed. We concluded that the miR-22-HDAC4-DLCO axis behaves differently in patients with COPD-BS and COPD-TS.
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Histona Desacetilases/metabolismo , MicroRNAs , Doença Pulmonar Obstrutiva Crônica/metabolismo , Fumar/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Estudos Transversais , Feminino , Humanos , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/etiologia , Proteínas Repressoras/metabolismo , Fumaça/efeitos adversos , NicotianaRESUMO
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities. The main causes of COPD are Gene-environment interactions associated with tobacco smoking (COPD-TS) and biomass smoke (COPD-BS). It is well know that microRNAs (miRNAs) participate in the control of post-transcriptional regulation and are involved in COPD-TS; nevertheless, those miRNAS are participating in the COPD-BS are unidentified. Thus, we studied which miRNAs are involved in COPD-BS (GOLD stages I-II). METHODS: In the screening phase, the profile of the miRNAs was analyzed in serum samples (n = 3) by means of a PCR array. Subsequently, the miRNAs were validated with RT-qPCR (n = 25) in the corresponding study groups. Additionally, the serum concentration of Notch1 was measured comparing COPD-BS vs COPD-TS. RESULTS: miR-34a was down-regulated in COPD- BS vs COPD-TS. In the other study groups, three miRNAs were differentially expressed: miR-374a was down-regulated in COPD-BS vs C, miR-191-5p was up-regulated in COPD-BS vs H-BS, and miR-21-5p was down-regulated in COPD-TS compared to the C group. Moreover, the serum concentration of Notch1, one of the targets of miR-34a, was increased in COPD-BS compared to women with COPD-TS. CONCLUSIONS: This is the first study in patients with COPD due to biomass that demonstrates miRNA expression differences between patients. The observations support the concept that COPD by biomass has a different phenotype than COPD due to tobacco smoking, which could have important implications for the treatment of these diseases.
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Biomassa , Exposição Ambiental , MicroRNAs/sangue , Doença Pulmonar Obstrutiva Crônica/sangue , Fumaça , Idoso , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/etiologia , Índice de Gravidade de Doença , Fumaça/efeitos adversosRESUMO
Human exposure to polycyclic aromatic hydrocarbons (PAHs) has been considered a risk determinant for the development of cardiovascular diseases (CVD). Therefore, the aim of this study was to assess expression levels of vascular-related miRNAs, miR-126, miR-155, and miR-145, in plasma from women (aged 19-81 years) exposed (n = 100) and non-exposed (n = 20) to PAHs via biomass combustion smoke.1-hydroxypyrene (1-OHP) was determined in urine as a biomarker of exposure to PAHs using high-resolution liquid chromatography. Plasma expression levels of proposed miRNAs were determined by quantitative real-time PCR. Additionally, traditional risk factors (age, blood pressure, serum lipid profile, blood glucose, and among others) associated with CVD were evaluated. Urinary 1-OHP concentrations and plasma expression levels of miR-126 and miR-155 were significantly higher (P < 0.05) in women using wood as a fuel source in their homes (indoor) compared to women from the reference group (non-exposed to biomass smoke). Besides, multivariate linear regression analyses revealed that miR-126[ß = 0.61; 95% confidence interval (0.32-0.90)] and miR-155 [ß = 0.45; 95% confidence interval (0.13-0.84)] expression levels were significantly associated with urinary 1-OHP concentrations after being adjusted by traditional risk factors (P < 0.05). In contrast, no significant relationship was found between miR-145 and urinary 1-OHP levels. Furthermore, miRNAs assessed in this investigation are associated with CVD events. Consequently, actions to reduce exposure to PAHs in the evaluated population are warranted. Environ. Mol. Mutagen. 60:546-558, 2019. © 2019 Wiley Periodicals, Inc.
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MicroRNA Circulante/genética , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/efeitos adversos , Biomassa , Estudos Transversais , Exposição Ambiental/efeitos adversos , Feminino , Humanos , México , Pessoa de Meia-Idade , Pirenos/efeitos adversos , Fatores de Risco , Fumaça/efeitos adversos , Madeira/efeitos adversos , Adulto JovemRESUMO
Household air pollution has been associated as a risk factor for cardiovascular diseases (CVD). Therefore, the aim of this study was to assess the expression of vascular inflammation regulators miR-126 and miR-155 in plasma from women that cook with wood and women that cook with liquid petroleum gas (LPG). A cumulative index of exposure to smoke (CIES) was estimated, urinary 1-hydroxypyrene (1-OHP) levels were quantified and miRNAs expression levels were determined by quantitative real-time PCR (qRT-PCR). Biochemical clinical parameters were also evaluated. The average values for CIES and 1-OHP were 140 ± 86.8 hours-years (12.0-270 hours-years) and 0.52 ± 0.45 µmol/mol creatinine, respectively. miR-126 and miR-155 expression levels were significantly higher (p < 0.01) in the wood users compared to LPG users. Besides, we found a significant association (p < 0.01) between miR-126 and miR-155 expression levels and CIES and urinary 1-OHP concentrations. These results contribute to the current evidence about the cardiovascular risk related to biomass smoke exposure, from an epigenetic level.
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Poluentes Atmosféricos/efeitos adversos , Exposição por Inalação/análise , MicroRNAs/sangue , Fumaça/efeitos adversos , Adulto , Culinária , Creatinina/urina , Feminino , Humanos , México , Projetos Piloto , Madeira/químicaRESUMO
BACKGROUND: The main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). COPD-TS is known to induce changes in adipokines, incretins, and peptide hormones, frequent biomarkers of inflammation; however, it is unknown if similar changes occur in COPD-BS. METHODS: Clinical and physiological characteristics, and serum concentration of C-peptide, ghrelin, GIP, GLP-1, glucagon, insulin, leptin, PAI-1, resistin, and visfatin were measured in women with COPD-BS, COPD-TS, and healthy controls. Data were compared with one-way ANOVA and Tukey's post hoc test; nonparametric were expressed as median (interquartile ranges), with Kruskal-Wallis and Dunn's post-hoc test. Multivariate analysis, age, BMI, MS, and FEV1% pred with levels of inflammatory mediators in COPD women. RESULTS: FEV1% pred, FVC% pred, and FEV1/FVC ratio were decremented in COPD. In COPD-TS increased C-peptide, ghrelin, GIP, GLP-1, and leptin, and reduced glucagon, PAI-1, resistin, and visfatin. In COPD-BS enlarged ghrelin, insulin, leptin, and PAI-1 comparatively with COPD-TS and control, while C-peptide and GLP-1 relatively with controls; conversely, glucagon, and resistin were reduced. Multivariate analysis showed association of ghrelin, insulin, PAI-1, and visfatin with BS exposure. CONCLUSIONS: women with COPD-BS have a distinct profile of adipokines, incretins, and peptide hormones, and specifically with ghrelin, insulin, PAI-1, and visfatin related to BS exposure.
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Adipocinas/sangue , Fumar Cigarros/sangue , Incretinas/sangue , Hormônios Peptídicos/sangue , Doença Pulmonar Obstrutiva Crônica/sangue , Fumantes , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Fumar Cigarros/epidemiologia , Feminino , Humanos , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/epidemiologiaRESUMO
BACKGROUND: Exposure to noxious gases and particles contained in both tobacco smoking (TS) and biomass smoke (BS) are well recognized environmental risk factors for chronic obstructive pulmonary disease (COPD). COPD is characterized by an abnormal inflammatory response, both in the pulmonary and systemic compartments. The differential effects of TS, BS or their combined exposure have not been well characterized yet. This study sought to compare the lung function characteristics and systemic inflammatory response in COPD patients exposed to TS, BS or their combination. METHODS: Sociodemographic, clinical and lung functional parameters were compared across 49 COPD patients with a history of smoking and no BS exposure (TS COPD), 31 never-smoker COPD patients with BS exposure (BS COPD), 46 COPD patients with a combined exposure (TS + BS COPD) and 52 healthy controls (HC) who have never been exposed neither to TS or BS. Blood cell counts, C-reactive protein (CRP), fibrinogen and immunoglobulin E (IgE) levels were quantified in all four groups. RESULTS: TS + BS COPD patients exhibited significantly lower oxygen saturation than the rest of groups (p < 0.01). Spirometry and diffusing capacity were significantly higher in BS than in TS or TS + BS patients. CRP levels were significantly higher in TS COPD patients than in BS COPD group (p < 0.05), whereas fibrinogen was raised in COPD patients with a history of smoking (TS and TS + BS) when compared to control subjects (p < 0.01). Finally, COPD patients with BS exposure (BS and BS + TS groups) showed higher IgE levels than TS and HC (p < 0.05). CONCLUSIONS: There are significant physiological and inflammatory differences between COPD patients with TS, BS and TS + BS exposures. The latter had worse blood oxygenation, whereas the raised levels of IgE in BS exposed patients suggests a differential Th2 systemic inflammatory pattern triggered by this pollutant.
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Biomassa , Exposição Ambiental/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/sangue , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Fumaça/efeitos adversos , Fumar Tabaco/efeitos adversos , Idoso , Idoso de 80 Anos ou mais , Feminino , Volume Expiratório Forçado/fisiologia , Humanos , Mediadores da Inflamação/sangue , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Espirometria/métodos , Espirometria/tendências , Fumar Tabaco/tendênciasRESUMO
Chronic obstructive pulmonary disease (COPD), a major cause of mortality and morbidity worldwide, is considered an archetypical disease of innate immunity, where inhaled particles and gases trigger an inflammatory response, favoring tissue proliferation in small airways and tissue destruction in lung parenchyma, in addition to the recruitment of immune cells to these compartments. Although cigarette smoking is still considered the main risk factor for developing COPD, the trend of proposing biomass smoke (BS) exposure as a principal risk factor is gaining importance, as around 3 billion people worldwide are exposed to this pollutant daily. A considerable amount of evidence has shown the potential of BS as an enhancer of lung inflammation. However, an impairment of some innate immune responses after BS exposure has also been described. Regarding the mechanisms by which biomass smoke alters the innate immune responses, three main classes of cell surface receptors-the TLRs, the scavenger receptors and the transient receptor potential channels-have shown the ability to transduce signals initiated after BS exposure. This article is an updated and comprehensive review of the immunomodulatory effects described after the interaction of BS components with these receptors.
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Biomassa , Pulmão/imunologia , Pneumonia/imunologia , Doença Pulmonar Obstrutiva Crônica/imunologia , Poluentes Atmosféricos/efeitos adversos , Animais , Humanos , Imunidade Inata , Irritantes/efeitos adversos , Pneumonia/epidemiologia , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Fatores de Risco , Fumaça/efeitos adversos , Fumar/efeitos adversosRESUMO
Chronic obstructive pulmonary disease (COPD) mortality and morbidity have increased significantly worldwide in recent decades. Although cigarette smoke is still considered the main risk factor for the development of the disease, estimates suggest that between 25% and 33% of COPD patients are non-smokers. Among the factors that may increase the risk of developing COPD, biomass smoke has been proposed as one of the most important, affecting especially women and children in developing countries. Despite the epidemiological evidence linking exposure to biomass smoke with adverse health effects, the specific cellular and molecular mechanisms by which this pollutant can be harmful for the respiratory and cardiovascular systems remain unclear. In this article we review the main pathogenic mechanisms proposed to date that make biomass smoke one of the major risk factors for COPD.